Protective effects of natural dietary antioxidants fisetin and hesperidin on chronic mild hyperhomocysteinemia-induced vascular dementia in wistar rats

2017 ◽  
Vol 381 ◽  
pp. 319 ◽  
Author(s):  
B. Hemanth Kumar ◽  
B. Dinesh Kumar ◽  
P.V. Diwan
Molecules ◽  
2021 ◽  
Vol 26 (16) ◽  
pp. 4720
Author(s):  
Arlindo César Matias Pereira ◽  
Helison de Oliveira Carvalho ◽  
Danna Emanuelle Santos Gonçalves ◽  
Karyny Roberta Tavares Picanço ◽  
Abrahão Victor Tavares de Lima Teixeira dos dos Santos ◽  
...  

This study aimed to evaluate and compare the effects of co-treatment with purified annatto oil (PAO) or its granules (GRA, Chronic®) with that of testosterone on the orchiectomy-induced osteoporosis in Wistar rats. After surgery, rats were treated from day 7 until day 45 with testosterone only (TES, 7 mg/kg, IM) or TES + PAO or GRA (200 mg/kg, p.o.). The following parameters were evaluated: food/water intake, weight, HDL, LDL, glucose, triglycerides (TG), total cholesterol (TC), alkaline phosphatase levels, blood phosphorus and calcium contents, femur weight, structure (through scanning electron microscopy), and calcium content (through atomic absorption spectrophotometry). Our results show that orchiectomy could significantly change the blood lipid profile and decrease bone integrity parameters. Testosterone reposition alone could improve some endpoints, including LDL, TC, bone weight, and bone calcium concentration. However, other parameters were not significantly improved. Co-treatment with PAO or GRA improved the blood lipid profile and bone integrity more significantly and improved some endpoints not affected by testosterone reposition alone (such as TG levels and trabeculae sizes). The results suggest that co-treatment with annatto products improved the blood lipid profile and the anti-osteoporosis effects of testosterone. Overall, GRA had better results than PAO.


2018 ◽  
Vol 17 (1) ◽  
pp. 69-73
Author(s):  
N. S. Shcherbak ◽  
M. A. Popovetskiy ◽  
G. Yu. Yukina ◽  
M. M. Galagudza

Curcumin presents antioxidant and anti-inflammatory properties and can be considered as a neuroprotector. Data on doses and duration of application of curcumin to achieve protective effects in various types of ischemic brain injury is controversial. The purpose was to study the neuroprotective properties of curcumin in the acute phase of ischemia in chronic cerebral hypoperfusion in rats. It is shown that a single application of curcumin (300 mg/kg, i.p.) is not has neuroprotective effect in the acute phase of ischemia in chronic hypoperfusion in Wistar rats. The results allow to conclude that the neuroprotective effect of a single application of curcumin.


2019 ◽  
Vol 26 (7) ◽  
pp. 1429-1435 ◽  
Author(s):  
Manjunatha Sammeturi ◽  
Althaf Hussain Shaik ◽  
Sasi Bhusana Rao Bongu ◽  
Srinivasulu Cheemanapalli ◽  
Altaf Mohammad ◽  
...  

Author(s):  
Pei Jiang

<p class="lead">In this study, puerarin derivatives were designed by adding an active acetonitrile group that inhibits cyclooxygenase-2 (COX-2) in order to enhance the anti-vascular dementia drug activity. The acetonitrile group was linked to puerarin at the 7/4 'positions by a phenolic hydroxyl to give 7-mono-and 7, 4' di-substituted derivatives of puerarin. These structures were confirmed by <sup>1</sup>H NMR spectroscopy and MS spectroscopy. We compared the affinity of puerarin derivatives and puerarin for cyclooxygenase-2 (COX-2) using molecular docking. In addition, the anti-vascular dementia activity of the developed puerarin derivatives was studied by water maze, novel object recognition, and the determination of inducible nitric oxide synthase (iNOS) enzyme activity at the cerebral cortex of mice. Experimental results showed that the puerarin derivatives have a good affinity for COX-2 with therapeutic effects against vascular dementia. The results of this study suggest that the protective effects of the puerarin derivatives against vascular dementia may be related to suppression of inflammation associated with ischemia-reperfusion injury through inhibition of COX-2.</p>


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